Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-10-13
pubmed:abstractText
The nonobese diabetic (NOD) mouse develops insulin-dependent type 1 diabetes in response to autoantibodies and T-cell attack directed against pancreatic islet cell antigens. Sera obtained from nondiabetic and diabetic female mice demonstrated a 1.4-fold increase in IgG levels when compared to BALB/c control animals. Nondiabetic and diabetic male mice had a 2.1- and 3-fold increase, respectively, in serum IgG levels over that of control mice. Seven of 11 non-diabetic and 7/10 diabetic sera from female NOD mice contained antibody to cytoplasmic or nuclear components of HEp-2 cells. Cytoplasmic staining revealed reaction against cytoskeletal and midbody structures. Punctate nuclear staining patterns with HEp-2 cells showed antibody reaction to the centriole, mitotic chromosomes, and nuclear rim. On the other hand, sera from BALB/c mice were negative for antibody staining of HEp-2 cells. Confirmation of the autoantibody nature of the NOD sera was obtained by antibody staining of nuclear structures from the mouse 3T3 fibroblast cell line, and by staining of salivary gland tissue sections. The nuclear and cytoplasmic staining patterns of diabetic NOD sera were reminiscent of the autoantibody staining patterns observed in Sjögren's syndrome and other inflammatory autoimmune connective tissue diseases.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0090-1229
pubmed:author
pubmed:issnType
Print
pubmed:volume
68
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
350-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Characterization of antinuclear autoantibodies present in the serum from nonobese diabetic (NOD) mice.
pubmed:affiliation
Department of Oral Biology, University of Florida, Gainesville 32610.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.